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== Medical applications == Vitamin E has been suggested as a supplement for helping many health conditions, mostly due to its antioxidant activity and potential to protect cells from oxidative damage. In the US, the vitamin is widely available as an over-the-counter supplement; however, medical evidence supporting its effectiveness and safety for treating or preventing a variety of health conditions is mixed. Vitamin E can also interact with some medications and other supplements.<ref name=GOVe /> Vitamin E has been studied as a treatment for skin health and skin ageing, immune function,<ref>{{cite journal | vauthors = Lee GY, Han SN | title = The Role of Vitamin E in Immunity | journal = Nutrients | volume = 10 | issue = 11 | pages = 1614 | date = November 2018 | pmid = 30388871 | pmc = 6266234 | doi = 10.3390/nu10111614 | doi-access = free | title-link = doi }}</ref> and managing conditions like cardiovascular disease<ref name="Mangione2022" /> or [[Alzheimer's disease]] (AD),<ref name="Wang2021"/> or certain types of cancer.<ref name="Mangione2022" /> Most studies have found limited or inconclusive benefits and the potential for some risks. It is most often recommended to obtain vitamin E through a balanced diet because high-dose supplementation may have health risks.<ref name=GOVe /> There is evidence that the sale of dietary supplement vitamin E has decreased by up to 33% following a report showing little or no effect of vitamin E in preventing cancer or cardiovascular disease.<ref name="Tilburt2008" /> In 2022, it was the 244th most commonly prescribed medication in the United States, with more than 1{{nbsp}}million prescriptions.<ref>{{cite web | title=The Top 300 of 2022 | url=https://clincalc.com/DrugStats/Top300Drugs.aspx | website=ClinCalc | access-date=30 August 2024 | archive-date=30 August 2024 | archive-url=https://web.archive.org/web/20240830202410/https://clincalc.com/DrugStats/Top300Drugs.aspx | url-status=live }}</ref><ref>{{cite web | title = Vitamin E Drug Usage Statistics, United States, 2013 - 2022 | website = ClinCalc | url = https://clincalc.com/DrugStats/Drugs/VitaminE | access-date = 30 August 2024 | archive-date = 24 September 2024 | archive-url = https://web.archive.org/web/20240924115107/https://clincalc.com/DrugStats/Drugs/VitaminE | url-status = live }}</ref> === All-cause mortality === Two [[meta-analysis|meta-analyses]] concluded that as a dietary supplement, vitamin E neither improved nor impaired all-cause mortality.<ref name=Abner2011>{{cite journal | vauthors = Abner EL, Schmitt FA, Mendiondo MS, Marcum JL, Kryscio RJ | title = Vitamin E and all-cause mortality: a meta-analysis | journal = Current Aging Science | volume = 4 | issue = 2 | pages = 158β70 | date = July 2011 | pmid = 21235492 | pmc = 4030744 | doi = 10.2174/1874609811104020158 }}</ref><ref name=Curtis2014>{{cite journal |vauthors=Curtis AJ, Bullen M, Piccenna L, McNeil JJ |title=Vitamin E supplementation and mortality in healthy people: a meta-analysis of randomised controlled trials |journal=Cardiovasc Drugs Ther |volume=28 |issue=6 |pages=563β73 |date=December 2014 |pmid=25398301 |doi=10.1007/s10557-014-6560-7 |s2cid=23820017 }}</ref> A meta-analysis of long-term clinical trials reported a non-significant 2% increase in all-cause mortality when alpha-tocopherol was the only supplement used. The same journal article reported a statistically significant 3% increase for results when alpha-tocopherol was used in combination with other nutrients (vitamin A, vitamin C, beta-carotene, selenium).<ref name=Bjelakovic2014 /> === Age-related macular degeneration === A [[Cochrane (organisation)|Cochrane]] review concluded that there were no changes seen for risk of developing [[macular degeneration|age-related macular degeneration]] (AMD) from long-term vitamin E supplementation and that supplementation may slightly increase the chances of developing late AMD.<ref>{{cite journal | vauthors = Evans JR, Lawrenson JG | title = Antioxidant vitamin and mineral supplements for preventing age-related macular degeneration | journal = The Cochrane Database of Systematic Reviews | volume = 2017 | pages = CD000253 | date = July 2017 | issue = 7 | pmid = 28756617 | pmc = 6483250 | doi = 10.1002/14651858.CD000253.pub4 }}</ref> === Cognitive impairment and Alzheimer's disease === Two meta-analyses reported lower vitamin E blood levels in AD people compared to healthy, age-matched people.<ref>{{cite journal | vauthors = Dong Y, Chen X, Liu Y, Shu Y, Chen T, Xu L, Li M, Guan X |title = Do low-serum vitamin E levels increase the risk of Alzheimer disease in older people? Evidence from a meta-analysis of case-control studies |journal = International Journal of Geriatric Psychiatry |volume = 33 |issue = 2 |pages = e257βe63 |date = February 2018 |pmid = 28833475 | doi = 10.1002/gps.4780 |s2cid = 44859128 }}</ref><ref name="Ashley2021">{{cite journal |vauthors=Ashley S, Bradburn S, Murgatroyd C |title=A meta-analysis of peripheral tocopherol levels in age-related cognitive decline and Alzheimer's disease |journal=Nutr Neurosci |volume=24 |issue=10 |pages=795β809 |date=October 2021 |pmid=31661399 |doi=10.1080/1028415X.2019.1681066 |url=}}</ref> However, a review of vitamin E supplementation trials concluded that there was insufficient evidence to state that supplementation reduced the risk of developing AD or slowed the progression of AD.<ref name="Wang2021">{{cite journal |vauthors=Wang W, Li J, Zhang H, Wang X, Zhang X |title=Effects of vitamin E supplementation on the risk and progression of AD: a systematic review and meta-analysis |journal=Nutr Neurosci |volume=24 |issue=1 |pages=13β22 |date=January 2021 |pmid=30900960 |doi=10.1080/1028415X.2019.1585506 |url=}}</ref> === Cancer === In a 2022 update of an earlier report, the [[United States Preventive Services Task Force]] recommended against the use of vitamin E supplements for the prevention of cardiovascular disease or cancer, concluding there was insufficient evidence to assess the balance of benefits and harms, yet also concluding with moderate certainty that there is no net benefit of supplementation.<ref name="Mangione2022">{{cite journal |vauthors=Mangione CM, Barry MJ, Nicholson WK, Cabana M, Chelmow D, Coker TR, Davis EM, Donahue KE, Doubeni CA, JaΓ©n CR, Kubik M, Li L, Ogedegbe G, Pbert L, Ruiz JM, Stevermer J, Wong JB |title=Vitamin, mineral, and multivitamin supplementation to prevent cardiovascular disease and cancer: US preventive services task force recommendation statement |journal=JAMA |volume=327 |issue=23 |pages=2326β33 |date=June 2022 |pmid=35727271 |doi=10.1001/jama.2022.8970 |s2cid=249886842 |url=| doi-access = free | title-link = doi }}</ref> As for literature on different types of cancer, an inverse relationship between dietary vitamin E and [[kidney cancer]] and [[bladder cancer]] is seen in observational studies.<ref>{{cite journal | vauthors = Shen C, Huang Y, Yi S, Fang Z, Li L | title = Association of vitamin E intake with reduced risk of kidney cancer: a meta-analysis of observational Studies | journal = Medical Science Monitor | volume = 21 | pages = 3420β6 | date = November 2015 | pmid = 26547129 | pmc = 4644018 | doi = 10.12659/MSM.896018 }}</ref><ref>{{cite journal | vauthors = Wang YY, Wang XL, Yu ZJ | title = Vitamin C and E intake and risk of bladder cancer: a meta-analysis of observational studies | journal = International Journal of Clinical and Experimental Medicine | volume = 7 | issue = 11 | pages = 4154β64 | date = 2014 | pmid = 25550926 | pmc = 4276184 }}</ref> A large clinical trial reported no difference in bladder cancer cases between treatment and placebo.<ref>{{cite journal | vauthors = Lotan Y, Goodman PJ, Youssef RF, Svatek RS, Shariat SF, Tangen CM, Thompson IM, Klein EA | title = Evaluation of vitamin E and selenium supplementation for the prevention of bladder cancer in SWOG coordinated SELECT | journal = The Journal of Urology | volume = 187 | issue = 6 | pages = 2005β10 | date = June 2012 | pmid = 22498220 | pmc = 4294531 | doi = 10.1016/j.juro.2012.01.117 }}</ref> An inverse relationship between dietary vitamin E and [[lung cancer]] was reported in observational studies,<ref>{{cite journal |vauthors = Zhu YJ, Bo YC, Liu XX, Qiu CG | title = Association of dietary vitamin E intake with risk of lung cancer: a dose-response meta-analysis |journal = Asia Pacific Journal of Clinical Nutrition |volume = 26 |issue = 2 | pages = 271β7 |date = March 2017 |pmid = 28244705 |doi = 10.6133/apjcn.032016.04 }}</ref> but a large clinical trial in male tobacco smokers reported no impact on lung cancer between treatment and placebo,<ref>{{cite journal | title = The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers | journal = The New England Journal of Medicine | volume = 330 | issue = 15 | pages = 1029β35 | date = April 1994 | pmid = 8127329 | doi = 10.1056/NEJM199404143301501 | vauthors = ((Alpha-Tocopherol)), ((Beta Carotene Cancer Prevention Study Group)) | doi-access = free | title-link = doi }}</ref> and a trial which tracked people who chose to consume a vitamin E dietary supplement reported an increased risk of lung cancer for those consuming more than 215 mg/day.<ref name="Slatore2008">{{cite journal | vauthors = Slatore CG, Littman AJ, Au DH, Satia JA, White E | title = Long-term use of supplemental multivitamins, vitamin C, vitamin E, and folate does not reduce the risk of lung cancer | journal = American Journal of Respiratory and Critical Care Medicine |volume = 177 |issue = 5 |pages = 524β30 |date = March 2008 |pmid = 17989343 |pmc = 2258445 |doi = 10.1164/rccm.200709-1398OC }}</ref> For [[prostate cancer]], there are also conflicting results. A meta-analysis based on serum alpha-tocopherol content reported an inverse correlation in relative risk,<ref>{{cite journal | vauthors = Cui R, Liu ZQ, Xu Q | title = Blood Ξ±-tocopherol, Ξ³-tocopherol levels and risk of prostate cancer: a meta-analysis of prospective studies | journal = PLOS ONE| volume = 9 | issue = 3 | pages = e93044 | date = 2014 | pmid = 24667740 | pmc = 3965522 | doi = 10.1371/journal.pone.0093044 | bibcode = 2014PLoSO...993044C | doi-access = free | title-link = doi }}</ref> but a second meta-analysis of observational studies reported no such relationship.<ref>{{cite journal | vauthors = Kim Y, Wei J, Citronberg J, Hartman T, Fedirko V, Goodman M | title = Relation of vitamin E and selenium exposure to prostate cancer risk by smoking Status: A Review and Meta-Analysis | journal = Anticancer Research | volume = 35 | issue = 9 | pages = 4983β96 | date = September 2015 | pmid = 26254398 }}</ref> A large clinical trial with male tobacco smokers and reported a 32% decrease in the incidence of prostate cancer,<ref>{{cite journal | vauthors = Heinonen OP, Albanes D, Virtamo J, Taylor PR, Huttunen JK, Hartman AM, Haapakoski J, Malila N, Rautalahti M, Ripatti S, MΓ€enpÀÀ H, Teerenhovi L, Koss L, Virolainen M, Edwards BK | title = Prostate cancer and supplementation with alpha-tocopherol and beta-carotene: incidence and mortality in a controlled trial | journal = Journal of the National Cancer Institute | volume = 90 | issue = 6 | pages = 440β6 | date = March 1998 | pmid = 9521168 | doi = 10.1093/jnci/90.6.440 | doi-access = free | title-link = doi }}</ref> but the SELECT trial of selenium or vitamin E for prostate cancer enrolled men ages 55 or older and reported relative risk 17% higher for the vitamin group.<ref>{{cite journal | vauthors = Klein EA, Thompson IM, Tangen CM, Crowley JJ, Lucia MS, Goodman PJ, Minasian LM, Ford LG, Parnes HL, Gaziano JM, Karp DD, Lieber MM, Walther PJ, Klotz L, Parsons JK, Chin JL, Darke AK, Lippman SM, Goodman GE, Meyskens FL, Baker LH | title = Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT) | journal = JAMA | volume = 306 | issue = 14 |pages = 1549β56 | date = October 2011 | pmid = 21990298 | pmc = 4169010 | doi = 10.1001/jama.2011.1437 }}</ref> For [[colorectal cancer]], a systematic review of randomized clinical trials and the large SELECT trial reported no statistically significant change in relative risk.<ref>{{cite journal | vauthors = Arain MA, Abdul Qadeer A | title = Systematic review on "vitamin E and prevention of colorectal cancer" | journal = Pakistan Journal of Pharmaceutical Sciences | volume = 23 | issue = 2 | pages = 125β30 | date = April 2010 | pmid = 20363687 }}</ref><ref>{{cite journal | vauthors = Lance P, Alberts DS, Thompson PA, Fales L, Wang F, San Jose J, Jacobs ET, Goodman PJ, Darke AK, Yee M, Minasian L, Thompson IM, Roe DJ | title = Colorectal adenomas in participants of the SELECT randomized trial of selenium and vitamin E for prostate cancer prevention | journal = Cancer Prevention Research | volume = 10 | issue = 1 | pages = 45β54 | date = January 2017 | pmid = 27777235 | pmc = 5510661 | doi = 10.1158/1940-6207.CAPR-16-0104 }}</ref> The Women's Health Study reported no significant differences for incidences of all types of cancer, cancer deaths, or specifically for breast, lung or colon cancers.<ref name="ReferenceA">{{cite journal | vauthors = Lee IM, Cook NR, Gaziano JM, Gordon D, Ridker PM, Manson JE, Hennekens CH, Buring JE | title = Vitamin E in the primary prevention of cardiovascular disease and cancer: the Women's Health Study: a randomized controlled trial |journal = JAMA | volume = 294 |issue = 1 | pages = 56β65 |date = July 2005 | pmid = 15998891 | doi = 10.1001/jama.294.1.56 }}</ref> Potential confounding factors are the form of vitamin E used in prospective studies and the amounts. Synthetic, racemic mixtures of vitamin E isomers are not bioequivalent to natural, non-racemic mixtures, yet are widely used in clinical trials and as dietary supplement ingredients.<ref>{{cite book | vauthors = Jensen SK, Lauridsen C | title = Alpha-tocopherol stereoisomers | volume = 76 | pages = 281β308 |year = 2007 |pmid = 17628178 | doi = 10.1016/S0083-6729(07)76010-7 |isbn = 978-0-12-373592-8 |series = Vitamins & Hormones |chapter = Ξ-Tocopherol Stereoisomers }}</ref> One review reported a modest increase in cancer risk with vitamin E supplementation while stating that more than 90% of the cited clinical trials used the synthetic, racemic form dl-alpha-tocopherol.<ref name="Slatore2008" /> ==== Cancer health claims ==== The U.S. Food and Drug Administration initiated a process of reviewing and approving food and dietary supplement health claims in 1993. Reviews of petitions results in proposed claims being rejected or approved. If approved, specific wording is allowed on package labels. In 1999, a second process for claims review was created. If there is not a scientific consensus on the totality of the evidence, a Qualified Health Claim (QHC) may be established. The FDA does not "approve" qualified health claim petitions. Instead, it issues a Letter of Enforcement Discretion that includes very specific claim language and the restrictions on using that wording.<ref>{{cite web |url=https://www.fda.gov/Food/LabelingNutrition/ucm2006877.htm |title=Qualified health claims |website=Overview from the US Food & Drug Administration |access-date=24 August 2018 |archive-date=7 September 2018 |archive-url=https://web.archive.org/web/20180907203827/https://www.fda.gov/Food/LabelingNutrition/ucm2006877.htm |url-status=live }}</ref> The first QHCs relevant to vitamin E were issued in 2003: "Some scientific evidence suggests that consumption of antioxidant vitamins may reduce the risk of certain forms of cancer." In 2009, the claims became more specific, allowing that vitamin E might reduce the risk of renal, bladder and colorectal cancers, but with required mention that the evidence was deemed weak and the claimed benefits highly unlikely. A petition to add brain, cervical, gastric and lung cancers was rejected. A further revision, May 2012, allowed that vitamin E may reduce risk of renal, bladder and colorectal cancers, with a more concise qualifier sentence added: "FDA has concluded that there is very little scientific evidence for this claim." Any company product label making the cancer claims has to include a qualifier sentence.<ref>{{cite web |url=https://www.fda.gov/Food/IngredientsPackagingLabeling/LabelingNutrition/ucm306866.htm |archive-url=https://wayback.archive-it.org/7993/20171114183722/https://www.fda.gov/Food/IngredientsPackagingLabeling/LabelingNutrition/ucm306866.htm |url-status=dead |archive-date=14 November 2017 |title=Alliance for Natural Health v. Sebelius, Case No. 09-1546 (D.D.C.) | date=2012 |website=US Food & Drug Administration |access-date=24 August 2018}}</ref> === Cataracts === A review measured serum tocopherol and reported higher serum concentration was associated with a 23% reduction in relative risk of age-related [[cataract]]s (ARC), with the effect due to differences in nuclear cataract rather than cortical or posterior subcapsular cataract.<ref name=Zhang2015>{{cite journal | vauthors = Zhang Y, Jiang W, Xie Z, Wu W, Zhang D | title = Vitamin E and risk of age-related cataract: a meta-analysis | journal = Public Health Nutrition | volume = 18 | issue = 15 | pages = 2804β14 | date = October 2015 | pmid = 25591715 | doi = 10.1017/S1368980014003115 | pmc = 10271701 | s2cid = 3168065 }}</ref> In contrast, meta-analyses reporting on clinical trials of alpha-tocopherol supplementation reported no statistically significant change to risk of ARC compared to placebo.<ref name=Zhang2015 /><ref>{{cite journal | vauthors = Mathew MC, Ervin AM, Tao J, Davis RM | title = Antioxidant vitamin supplementation for preventing and slowing the progression of age-related cataract | journal = The Cochrane Database of Systematic Reviews | volume = 2012 | issue = 6 | pages = CD004567 | date = June 2012 | pmid = 22696344 | pmc = 4410744 | doi = 10.1002/14651858.CD004567.pub2 }}</ref> === Cardiovascular diseases === In a 2022 update of an earlier report, the [[United States Preventive Services Task Force]] recommended against the use of vitamin E supplements for the prevention of cardiovascular disease or cancer, concluding there was insufficient evidence to assess the balance of benefits and harms, yet also concluding with moderate certainty that there is no net benefit of supplementation.<ref name="Mangione2022" /> Research on the effects of vitamin E on [[cardiovascular disease]] has produced conflicting results. In theory, oxidative modification of [[Low-density lipoprotein|LDL-cholesterol]] promotes blockages in coronary arteries that lead to [[atherosclerosis]] and [[myocardial infarction|heart attacks]], so vitamin E functioning as an antioxidant would reduce oxidized cholesterol and lower risk of cardiovascular disease. Vitamin E status has also been implicated in the maintenance of normal endothelial cell function of cells lining the inner surface of arteries, anti-inflammatory activity and inhibition of [[platelet]] adhesion and aggregation.<ref name=Kirmizis2009>{{cite journal | vauthors = Kirmizis D, Chatzidimitriou D | title = Antiatherogenic effects of vitamin E: the search for the Holy Grail | journal = Vascular Health and Risk Management | volume = 5 | pages = 767β74 | date = 2009 | pmid = 19774218 | pmc = 2747395 | doi = 10.2147/vhrm.s5532 | doi-access = free | title-link = doi }}</ref> An inverse relation has been observed between [[coronary heart disease]] and the consumption of foods high in vitamin E, and also higher serum concentration of alpha-tocopherol.<ref name=Kirmizis2009 /><ref>{{cite journal | vauthors = Gaziano JM | title = Vitamin E and cardiovascular disease: observational studies | journal = Annals of the New York Academy of Sciences | volume = 1031 | issue = 1 |pages = 280β91 |date = December 2004 | pmid = 15753154 | doi = 10.1196/annals.1331.028 | bibcode = 2004NYASA1031..280G | s2cid = 26369772 }}</ref> The problem with observational studies is that these cannot confirm a relation between the lower risk of coronary heart disease and vitamin E consumption diets higher in vitamin E may also be higher in other, unidentified components that promote heart health, or lower in diet components detrimental to heart health, or people choosing such diets may be making other healthy lifestyle choices.<ref name=Kirmizis2009 /> A meta-analysis of [[randomized clinical trial]]s (RCTs) reported that when consumed without any other antioxidant nutrient, the relative risk of heart attack was reduced by 18%.<ref name=Loffredo2015>{{cite journal | vauthors = Loffredo L, Perri L, Di Castelnuovo A, Iacoviello L, De Gaetano G, Violi F | title = Supplementation with vitamin E alone is associated with reduced myocardial infarction: a meta-analysis | journal = Nutrition, Metabolism, and Cardiovascular Diseases | volume = 25 | issue = 4 | pages = 354β63 | date = April 2015 | pmid = 25779938 | doi = 10.1016/j.numecd.2015.01.008 }}</ref> However, two large trials that were incorporated into the meta-analysis either did not show any benefit for heart attack, stroke, coronary mortality or all-cause mortality,<ref name=Sesso2008>{{cite journal | vauthors = Sesso HD, Buring JE, Christen WG, Kurth T, Belanger C, MacFadyen J, Bubes V, Manson JE, Glynn RJ, Gaziano JM |title = Vitamins E and C in the prevention of cardiovascular disease in men: the Physicians' Health Study II randomized controlled trial | journal = JAMA |volume = 300 |issue = 18 |pages = 2123β33 | date = November 2008 | pmid = 18997197 | pmc = 2586922 | doi = 10.1001/jama.2008.600 }}</ref> or else a higher risk of heart failure in the alpha-tocopherol group.<ref>{{cite journal | vauthors = Lonn E, Bosch J, Yusuf S, Sheridan P, Pogue J, Arnold JM, Ross C, Arnold A, Sleight P, Probstfield J, Dagenais GR | title = Effects of long-term vitamin E supplementation on cardiovascular events and cancer: a randomized controlled trial | journal = JAMA | volume = 293 | issue = 11 | pages = 1338β47 | date = March 2005 | pmid = 15769967 | doi = 10.1001/jama.293.11.1338 | doi-access = free | title-link = doi }}</ref> Vitamin E supplementation does not reduce the incidence of [[Brain ischemia|ischemic]] or [[Intracerebral hemorrhage|hemorrhagic]] [[stroke]].<ref>{{cite journal | vauthors = Bin Q, Hu X, Cao Y, Gao F | title = The role of vitamin E (tocopherol) supplementation in the prevention of stroke. A meta-analysis of 13 randomized controlled trials | journal = Thrombosis and Haemostasis| volume = 105 | issue = 4 | pages = 579β85 | date = April 2011 | pmid = 21264448 | doi = 10.1160/TH10-11-0729 | s2cid = 23237227 }}</ref><ref name=Maggio2024/> However, supplementation of vitamin E with other antioxidants reduced risk of ischemic stroke by 9% while increased the risk for hemorrhagic stroke by 22%.<ref name=Maggio2024>{{cite journal |vauthors=Maggio E, Bocchini VP, Carnevale R, Pignatelli P, Violi F, Loffredo L |title=Vitamin E supplementation (alone or with other antioxidants) and stroke: a meta-analysis |journal=Nutr Rev |volume=82 |issue=8 |pages=1069β78 |date=August 2024 |pmid=37698992 |doi=10.1093/nutrit/nuad114 |url=}}</ref> ==== Denial of cardiovascular health claims ==== In 2001, the U.S. [[Food and Drug Administration]] rejected proposed health claims for vitamin E and cardiovascular health.<ref>{{cite web |url=https://www.fda.gov/Food/IngredientsPackagingLabeling/LabelingNutrition/ucm073251.htm |archive-url=https://wayback.archive-it.org/7993/20171115122059/https://www.fda.gov/Food/IngredientsPackagingLabeling/LabelingNutrition/ucm073251.htm |url-status=dead |archive-date=15 November 2017 |title=Letter regarding dietary supplement health claim for vitamin E and heart disease (Docket No 99P-4375) |website=U.S. Food and Drug Administration |access-date=24 August 2018}}</ref> The U.S. National Institutes of Health reviewed literature published up to 2008 and concluded "In general, clinical trials have not provided evidence that routine use of vitamin E supplements prevents cardiovascular disease or reduces its morbidity and mortality."<ref name="GOVe" /> The [[European Food Safety Authority]] (EFSA) reviews proposed health claims for the [[European Union]] countries. In 2010, the EFSA reviewed and rejected claims that a cause and effect relationship has been established between the dietary intake of vitamin E and maintenance of normal cardiac function or of normal blood circulation.<ref>{{cite journal |doi=10.2903/j.efsa.2010.1816 |title=Scientific Opinion on the substantiation of health claims related to vitamin E and protection of DNA, proteins and lipids from oxidative damage (ID 160, 162, 1947), maintenance of the normal function of the immune system (ID 161, 163), maintenance of normal bone (ID 164), maintenance of normal teeth (ID 164), maintenance of normal hair (ID 164), maintenance of normal skin (ID 164), maintenance of normal nails (ID 164), maintenance of normal cardiac function (ID 166), maintenance of normal vision by protection of the lens of the eye (ID 167), contribution to normal cognitive function (ID 182, 183), regeneration of the reduced form of vitamin C (ID 203), maintenance of normal blood circulation (ID 216) and maintenance of normal a scalp (ID 2873) pursuant to Article 13(1) of Regulation (EC) No 1924/2006 |journal=EFSA Journal |volume=8 |issue=10 |pages=1816 |year=2010 | doi-access = free | title-link = doi }}</ref> === Nonalcoholic fatty liver disease === Supplemental vitamin E significantly reduced elevated liver enzymes, [[steatosis]], inflammation and fibrosis, suggesting that the vitamin may be useful for treatment of [[nonalcoholic fatty liver disease]] (NAFLD) and the more extreme subset known as nonalcoholic [[steatohepatitis]] (NASH) in adults,<ref name=Sato2015>{{cite journal | vauthors = Sato K, Gosho M, Yamamoto T, Kobayashi Y, Ishii N, Ohashi T, Nakade Y, Ito K, Fukuzawa Y, Yoneda M | title = Vitamin E has a beneficial effect on nonalcoholic fatty liver disease: a meta-analysis of randomized controlled trials | journal = Nutrition | volume = 31 | issue = 7β8 | pages = 923β30 | date = 2015 | pmid = 26059365 | doi = 10.1016/j.nut.2014.11.018 }}</ref><ref>{{cite journal |vauthors=Vadarlis A, Antza C, Bakaloudi DR, Doundoulakis I, Kalopitas G, Samara M, Dardavessis T, Maris T, Chourdakis M |title=Systematic review with meta-analysis: The effect of vitamin E supplementation in adult patients with non-alcoholic fatty liver disease |journal=J Gastroenterol Hepatol |volume=36 |issue=2 |pages=311β19 |date=February 2021 |pmid=32810309 |doi=10.1111/jgh.15221 |s2cid=221181369 }}</ref><ref>{{cite journal |vauthors=Wang MY, Prabahar K, GΔman MA, Zhang JL |title=Vitamin E supplementation in the treatment on nonalcoholic fatty liver disease (NAFLD): Evidence from an umbrella review of meta-analysis on randomized controlled trials |journal=J Dig Dis |volume=24 |issue=6β7 |pages=380β89 |date=2023 |pmid=37503812 |doi=10.1111/1751-2980.13210 |url=}}</ref> but not in children.<ref>{{cite journal |vauthors=Amanullah I, Khan YH, Anwar I, Gulzar A, Mallhi TH, Raja AA |title=Effect of vitamin E in non-alcoholic fatty liver disease: a systematic review and meta-analysis of randomized controlled trials |journal=Postgrad Med J |volume=95 |issue=1129 |pages=601β11 |date=November 2019 |pmid=31434683 |doi=10.1136/postgradmedj-2018-136364 |s2cid=201275520 |url=| doi-access = free | title-link = doi }}</ref><ref>{{cite journal |vauthors=Lin M, Zeng H, Deng G, Lei J, Li J |title=Vitamin E in pediatric non-alcoholic fatty liver disease: a meta-analysis |journal=Clin Res Hepatol Gastroenterol |volume=45 |issue=3 |pages=101530 |date=May 2021 |pmid=33272889 |doi=10.1016/j.clinre.2020.08.008 |s2cid=227282863 }}</ref> ===Exercise recovery=== In healthy adults, after exercise, vitamin E was shown to not have any benefits for post-exercise recovery, as measured by muscle soreness and muscle strength, or measured by indicators for inflammation or muscle damage, such as [[interleukin-6]] and [[creatine kinase]].<ref name=Lima2024>{{cite journal |vauthors=de Lima KS, Schuch F, Righi NC, Neto LJ, Nunes GS, Puntel G, Chagas P, da Silva AM, Signori LU |title=Vitamin E Does not Favor Recovery After Exercises: Systematic Review and Meta-analysis |journal=Int J Sports Med |volume=45 |issue=7 |pages=485β95 |date=June 2024 |pmid=38346687 |doi=10.1055/a-2221-5688 |url=}}</ref> === Parkinson's disease === For [[Parkinson's disease]], there is an observed inverse correlation seen with dietary vitamin E, but no confirming evidence from placebo-controlled clinical trials.<ref>{{cite journal | vauthors = Etminan M, Gill SS, Samii A | title = Intake of vitamin E, vitamin C, and carotenoids and the risk of Parkinson's disease: a meta-analysis | journal = The Lancet. Neurology | volume = 4 | issue = 6 | pages = 362β5 | date = June 2005 | pmid = 15907740 | doi = 10.1016/S1474-4422(05)70097-1 | s2cid = 25691968 }}</ref><ref>{{cite journal |vauthors=Chang MC, Kwak SG, Kwak S |title=Effect of dietary vitamins C and E on the risk of Parkinson's disease: A meta-analysis |journal=Clin Nutr |volume=40 |issue=6 |pages=3922β30 |date=June 2021 |pmid=34139465 |doi=10.1016/j.clnu.2021.05.011 |s2cid=235470579 }}</ref> === Pregnancy === Supplementation with a combination of vitamins E and C during pregnancy is not recommended by the [[World Health Organization]].<ref name=":0">{{Cite web |title=Vitamin E and C supplementation during pregnancy |url=https://www.who.int/tools/elena/interventions/vitaminsec-pregnancy |date=August 2023 |access-date=21 October 2024 |website=[[World Health Organization]] |archive-date=27 November 2024 |archive-url=https://web.archive.org/web/20241127221649/https://www.who.int/tools/elena/interventions/vitaminsec-pregnancy |url-status=live }}</ref> A Cochrane review concluded there was no support for the combination reducing risk of [[stillbirth]], [[neonatal death]], [[preterm birth]], [[preeclampsia]], or any other maternal or infant outcomes, either in healthy women or those considered at risk for pregnancy complications.<ref name=CochraneVitE>{{cite journal | vauthors = Rumbold A, Ota E, Hori H, Miyazaki C, Crowther CA | title = Vitamin E supplementation in pregnancy | journal = The Cochrane Database of Systematic Reviews | issue = 9 | pages = CD004069 | date = September 2015 | volume = 2016 | pmid = 26343254 | doi = 10.1002/14651858.CD004069.pub3 | pmc = 8406700 }}</ref> ===Topical applications=== There is widespread use of [[tocopheryl acetate]] in some [[cosmetics|skincare]] and wound-treatment products as a [[topical medication]], with claims for improved [[wound healing]] and reduced [[scar]] tissue,<ref name=Panin2004>{{cite journal | vauthors = Panin G, Strumia R, Ursini F | title = Topical alpha-tocopherol acetate in the bulk phase: eight years of experience in skin treatment | journal = Annals of the New York Academy of Sciences | volume = 1031 | issue = 1 | pages = 443β7 | date = December 2004 | pmid = 15753192 | doi = 10.1196/annals.1331.069 | bibcode = 2004NYASA1031..443P | s2cid = 45771699 }}</ref> but reviews have repeatedly concluded that there is insufficient evidence to support these claims.<ref name=Sidgwick2015>{{cite journal |vauthors = Sidgwick GP, McGeorge D, Bayat A |title = A comprehensive evidence-based review on the role of topicals and dressings in the management of skin scarring |journal = Archives of Dermatological Research |volume = 307 |issue = 6 |pages = 461β77 |date = August 2015 |pmid = 26044054 | pmc = 4506744 |doi = 10.1007/s00403-015-1572-0}}</ref><ref name=Tanaydin2016>{{cite journal | vauthors = Tanaydin V, Conings J, Malyar M, van der Hulst R, van der Lei B | title = The role of topical vitamin E in scar management: a systematic review | journal = Aesthetic Surgery Journal | volume = 36 | issue = 8 | pages = 959β65 | date = September 2016 | pmid = 26977069 | doi = 10.1093/asj/sjw046 | doi-access = free | title-link = doi }}</ref> There are also reports of allergic contact dermatitis from use of vitamin-E derivatives such as tocopheryl linoleate and tocopherol acetate in skin care products.<ref name=Kosari2010>{{cite journal | vauthors = Kosari P, Alikhan A, Sockolov M, Feldman SR | title = Vitamin E and allergic contact dermatitis | journal = Dermatitis | volume = 21 | issue = 3 | pages = 148β53 | date = 2010 | pmid = 20487657 | doi = 10.2310/6620.2010.09083| s2cid = 38212099 }}</ref>
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